Cereals, Phytic Acid and Teeth: The Mellanbys' Food Science

Edward Mellanby (1884–1955) is remembered for showing that cod liver oil prevents rickets. Less well known is the second half of the same story: the foods that made rickets worse. In his dog experiments the diets that produced the disease were heavy in oatmeal porridge, and over the next thirty years Mellanby and his co-workers kept returning to the question of why cereals interfered with the growth of bone. The answer they arrived at was a natural substance in the outer layers of grain, phytic acid, which binds calcium in the gut. Alongside him, his wife May Mellanby (1882–1978) spent decades studying how diet shapes the structure of teeth and the incidence of tooth decay, work that the Nobel Committee judged prize-worthy.

This page follows that food science in order: the fats that protected against rickets, the puzzle of oatmeal, the rat technique of 1928, the identification of phytic acid in 1939 and its anti-calcifying action described in 1949, the discovery of vitamin D activity in ergot of rye, May Mellanby’s research on teeth and her Nobel nominations, and finally what food scientists today report about phytate. The dog experiments themselves are told on the rickets experiments page, and the couple’s lives on the life and career page.

Table of Contents

  1. Fats That Prevented Rickets
  2. The Puzzle of Oatmeal
  3. A Rat Technique for Cereals and Bone (1928)
  4. Phytic Acid Identified (1939)
  5. How Phytate Binds Calcium
  6. Vitamin D in Ergot of Rye
  7. May Mellanby and the Structure of Teeth
  8. Diet, Cereals and Dental Caries
  9. A Nobel-Worthy Partner
  10. Phytate in Today’s Food Science
  11. Key Research Papers
  12. Connections

1. Fats That Prevented Rickets

Rickets is a disease of growing bone. In a child with rickets the soft framework of new bone is laid down but is not properly hardened with calcium and phosphate, so the long bones bend under the body’s weight, the wrists and ankles thicken, and the ends of the ribs swell into the “rickety rosary”. At the beginning of the twentieth century the disease was common among poor children in the smoky industrial cities of Britain and the northern United States, and its cause was disputed. Physicians blamed faulty diet, or a faulty environment — poor hygiene, lack of fresh air and sunshine — or lack of exercise.

Folk medicine had its own answer long before the laboratory did. Cod liver oil had been given to rickety children in parts of northern Europe for generations, and the pediatric historian Kumaravel Rajakumar lists this folklore, alongside animal experiments and the geographical link between rickets and lack of sunshine, among the threads that eventually solved the disease.

Mellanby’s contribution, published in The Lancet in 1919, was to turn the folklore into a controlled experiment. Working for the newly formed Medical Research Committee, he raised puppies on a restricted diet in which oatmeal porridge was a large part, and they developed rickets. When cod liver oil was added, the disease was prevented or cured. Other fats, butter among them, also protected. Mellanby concluded that rickets was a deficiency disease caused by the lack of a fat-soluble “accessory food factor”, one that was abundant in certain natural fats.

A natural source before a vitamin had a name

At the time Mellanby believed the protective factor was the fat-soluble vitamin A, which had recently been described and which is also plentiful in cod liver oil. It was Elmer McCollum’s group in the United States who, in 1922, separated a distinct calcium-depositing factor from vitamin A; it became vitamin D. Mellanby’s fats were therefore the first experimental proof that the antirachitic substance lived in food, and especially in fish liver oil, even before anyone knew which molecule it was. The physician-historian Russell Chesney places these dog experiments among the early animal models that proved the nutritional-deficiency theory of rickets.

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2. The Puzzle of Oatmeal

A curious detail ran through the dog work from the start. The diets that produced rickets most readily were built on cereal, above all oatmeal. Oatmeal porridge was a staple of the British diet, regarded as wholesome and nourishing. If cereals were simply neutral filler, they would have had no part in the disease; the lack of the fat-soluble factor alone would explain it. Mellanby came to suspect that this was not the whole story, and that the cereal in the diet was itself making matters worse.

This suggested that cereals were doing something active — that they contained a substance working against the calcifying action of the fat-soluble factor. Mellanby’s biographer B. J. Hawgood summarises the conclusion his Sheffield laboratory eventually reached: cereals in an unbalanced diet produced rickets because a component of the grain reduced the availability of calcium. The Royal College of Physicians’ obituary lists “cereals antagonising vitamin D” among the main lines of research Mellanby pursued after he took the chair of pharmacology at Sheffield in 1920.

The idea was controversial. Cereals were cheap, filling and central to the diets of the poor, and to suggest that a familiar food could actively encourage a deficiency disease ran against both popular belief and the hygiene-centred view of rickets held by many clinicians of the time. The controversy itself, and the opposition from Glasgow, are covered on the rickets experiments page.

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3. A Rat Technique for Cereals and Bone (1928)

Dogs were slow and expensive to study. Each experiment took weeks, needed a field laboratory and could include only a handful of animals. To test many cereals and many preparations of them, Mellanby needed a smaller, faster model. In 1928 he and H. N. Green, working in the Department of Pharmacology at Sheffield University, published in the Biochemical Journal “A rat technique for demonstrating the interfering effect of cereals on bone calcification.”

The title states the purpose plainly. The paper set out a way of using young rats to show, under controlled laboratory conditions, the effect that Mellanby had first seen in puppies: that cereals interfere with the deposit of calcium salts in growing bone. Rats were already the standard animal of nutrition research, used by McCollum and others in the vitamin work of the previous decade, and a rat method meant that the cereal effect could be measured on more animals, more quickly, and compared directly between grains and between different ways of preparing them.

It was the kind of patient, method-building work that seldom makes headlines but that made the later chemical answer possible: before one can find the substance in cereal that interferes with bone, one needs a reliable way of measuring the interference.

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4. Phytic Acid Identified (1939)

The chemical answer came in 1939. In a long paper in the Biochemical Journal, “Phytic acid and the rickets-producing action of cereals”, D. C. Harrison and Edward Mellanby identified phytic acid as the rickets-producing factor in cereals. Harrison was based in the Department of Biochemistry at Queen’s University, Belfast, and the work was carried out with the Field Laboratory of the University of Sheffield, a collaboration between a chemist and the physiologist’s animal laboratory.

Phytic acid was not a new substance to chemists; it was known as a phosphorus-rich compound present in seeds. What Harrison and Mellanby added was the link to disease: the substance that made oatmeal and other cereals rickets-producing in their experimental animals was phytic acid itself. This turned a vague observation — “cereals seem to make rickets worse” — into a specific mechanism that could be studied, measured and argued about.

The 1949 paper on phytate

Ten years later, by then long into his years as Secretary of the Medical Research Council and still doing laboratory work at weekends, Mellanby published a forty-six-page paper in the Journal of Physiology with two plates: “The rickets-producing and anti-calcifying action of phytate.” Its title sums up the conclusion of the whole thirty-year line of research. Phytate (the salt form of phytic acid) was described as both rickets-producing and anti-calcifying — that is, as acting directly against the hardening of bone with calcium.

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5. How Phytate Binds Calcium

Phytic acid is the main storage form of phosphorus in cereals, legumes, oilseeds and nuts. Chemically it is a ring of inositol (a sugar-like molecule) carrying six phosphate groups, which is why it is also called inositol hexakisphosphate. A seed stores phosphorus this way to feed the young plant when it sprouts. In whole grains the phytate is concentrated in the outer bran layers and the germ.

Those six phosphate groups carry negative charges, and in the digestive tract they grip positively charged minerals — calcium, iron, zinc and magnesium — forming complexes that the intestine absorbs poorly. Food scientists describe this as chelation. Ruminant animals such as cattle have gut microbes that break phytate down, but humans and other monogastric animals carry little of the enzyme phytase in their own digestive tracts, so in them much of the phytate passes through still holding its minerals.

Why this fits the rickets experiments

Seen through that chemistry, the Mellanby findings line up. A growing puppy on a diet poor in vitamin D absorbs calcium inefficiently to begin with. Add a large amount of oatmeal, rich in phytate, and some of the calcium that is present is bound in the gut and lost. Bone is starved of calcium from two directions at once, and rickets appears sooner and more severely. A fat rich in the antirachitic factor, such as cod liver oil, raises calcium absorption and works against the effect, which is why the Royal College of Physicians’ obituary could describe the Sheffield finding as cereals “antagonising” vitamin D.

This is also why the Mellanbys spoke of a balance in the diet rather than of good and bad foods. Hawgood’s summary is careful on the point: it was cereals in an unbalanced diet, poor in the fat-soluble factor and in calcium, that produced rickets.

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6. Vitamin D in Ergot of Rye

The cereal story had an unexpected side branch. Ergot is the dark, horn-shaped growth of the fungus Claviceps purpurea that replaces the grain in an infected ear of rye. It is famous in medical history for two reasons: it caused ergotism, the poisoning outbreaks of the Middle Ages known as St Anthony’s fire, and it was the natural source from which pharmacologists later obtained ergometrine and other ergot alkaloids. It also gave its name to ergosterol, a fungal sterol first isolated from ergot.

By the late 1920s other laboratories had shown that ergosterol, when irradiated with ultraviolet light, becomes antirachitic — the route to what would be called vitamin D2. In 1929 Edward Mellanby, E. Surie and D. C. Harrison, writing from the Pharmacology Department at Sheffield, published “Vitamin D in ergot of rye” in the Biochemical Journal, reporting vitamin D activity in the ergot itself.

The finding sits neatly in the natural-source thread of Mellanby’s work. Cod liver oil from the sea, butter from the farm, and a fungus growing on rye each turned out to carry antirachitic activity. It was a reminder that the same field could hold a grain whose phytate worked against bone and a fungus on that grain that carried an antirachitic factor. Ergot itself remains a poisonous growth; its interest here is purely as a chapter in the chemistry of vitamin D.

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7. May Mellanby and the Structure of Teeth

May Tweedy was a physiologist at Bedford College, London, who had met Edward Mellanby at Cambridge; they married in 1914 and worked side by side for the rest of his life. In 1918 she began dental research for the Medical Research Council, and over the following decades it became her own field. Where Edward studied the calcification of bone, May studied the calcification of teeth.

Her first major paper appeared in a dental journal in 1919: “An experimental study of the influence of diet on teeth formation.” As the title says, it was an experimental study of how the food eaten while teeth are forming affects the teeth that result. Teeth, like bone, are built of a protein framework hardened with calcium phosphate, so the same questions that drove her husband’s rickets work — the fat-soluble factor that would soon be named vitamin D, and the cereal content of the diet — applied to them as well.

She went on to publish four volumes in the Medical Research Council’s Special Report Series on diet and teeth, building a body of experimental and clinical work. Her work treated a well-formed tooth as the product of good nutrition during development, not simply as the result of how it was cleaned afterwards.

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8. Diet, Cereals and Dental Caries

In 1929 May Mellanby published in the Transactions of the Edinburgh Obstetrical Society “The effect of diet (antenatal and postnatal) on the structure of the teeth and the incidence of dental caries.” The title shows how far her research had reached by then. It was no longer only about the teeth of experimental animals: it took in the diet of the mother during pregnancy, the diet of the child after birth, the microscopic structure of the teeth that resulted, and how often those teeth later decayed.

The dietary pattern she favoured, as summarised in accounts of her work, was one rich in vitamin D and low in cereals — the same two levers that her husband had found in the rickets experiments. A diet rich in the antirachitic factor supported the calcification of developing teeth; a diet heavy in cereal, with its phytate, worked against it. Her 1929 title joins the two ends of the chain: the structure of the tooth and how often it decayed.

The wider debate about tooth decay

Her work entered a crowded field. Dental researchers of the period argued over whether decay was driven mainly by the structure of the tooth, by food residues and bacteria on its surface, or by the overall diet, and other investigators, among them the American dentist Weston Price, were drawing their own conclusions about traditional diets and teeth during the same years. Today’s dental science gives a large role to free sugars and the bacteria that ferment them; the Mellanbys’ research belongs to the earlier chapter that established that nutrition during development shapes how the tooth is built.

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9. A Nobel-Worthy Partner

In 2022 three historians of medicine at Heinrich Heine University Düsseldorf — L. Hense, A. Hugger and N. Hansson — went into the archive of the Nobel Committee to ask why no dentist has ever received a Nobel Prize. They reviewed the scholars in dental research who were nominated for the Nobel Prize in Physiology or Medicine between 1901 and 1950, focusing on two of them: the dentist Walter Hess and Lady May Mellanby.

Their finding about May Mellanby is striking. Hess never reached the committee’s shortlist, but Mellanby was judged “prize-worthy” by the Nobel Committee for Physiology or Medicine. She never received the award. The historians discuss what her work meant to the dentists of her day.

The title “Lady” came from Edward’s knighthood in 1937; her scientific reputation was her own. She outlived her husband by more than twenty years, dying in 1978. Accounts of the couple describe a partnership in which the two research programmes — his on bone, hers on teeth — ran in parallel and drew on the same discoveries about the fat-soluble factor and cereals.

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10. Phytate in Today’s Food Science

Phytate is still studied intensively, and modern reviews describe a more two-sided picture than the rickets work alone suggested. A 2009 review by Ulrich Schlemmer and colleagues in Molecular Nutrition & Food Research summarises the food sources and daily intake of phytate, how it is partly broken down during passage through the gut, how it interacts with minerals and trace elements in the intestinal contents, and its effects on mineral bioavailability. The same review also reports beneficial activities attributed to dietary phytate: effects on calcification and kidney-stone formation, lowering of blood glucose and lipids, antioxidant properties and possible anticancer activities.

A 2015 review by R. K. Gupta and colleagues in the Journal of Food Science and Technology focuses on the mineral side. It describes phytic acid as the major storage form of phosphorus in cereals, legumes, oilseeds and nuts, notes that it chelates micronutrients and that humans lack phytase in the digestive tract, and links it to the iron and zinc deficiencies that affect large populations in developing countries. It lists the methods developed to reduce phytate in grain: fermentation, soaking, germination (sprouting), enzymatic treatment with phytase, plant breeding and biofortification.

Traditional preparation

Those processing methods echo very old kitchen practices: soaking grains and legumes, sourdough fermentation of bread, sprouting seeds. The site’s page on soaking, sprouting and fermenting follows that tradition. Seen from today, Mellanby’s phytate research is one of the earliest scientific accounts of why such preparation can matter for minerals — while current research also describes phytate as a compound with its own reported benefits, so that its overall effect depends on the rest of the diet, much as Hawgood’s phrase “an unbalanced diet” implied.

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Key Research Papers

  1. Mellanby E. An experimental investigation on rickets. The Lancet. 1919;193:407-412. DOI: 10.1016/s0140-6736(01)25465-8
  2. Green HN, Mellanby E. A rat technique for demonstrating the interfering effect of cereals on bone calcification. Biochem J. 1928;22(1):102-12. PubMed PMID: 16743983
  3. Mellanby E, Surie E, Harrison DC. Vitamin D in ergot of rye. Biochem J. 1929;23(4):710-7. PubMed PMID: 16744257
  4. Harrison DC, Mellanby E. Phytic acid and the rickets-producing action of cereals. Biochem J. 1939;33(10):1660-1680.1. PubMed PMID: 16747083
  5. Mellanby E. The rickets-producing and anti-calcifying action of phytate. J Physiol. 1949;109(3-4):488-533. PubMed PMID: 15395027
  6. Mellanby M. An Experimental Study of the Influence of Diet on Teeth Formation. Dent Regist. 1919;73(5):231-242. PubMed PMID: 33703420
  7. Mellanby M. The Effect of Diet (Antenatal and Postnatal) on the Structure of the Teeth and the Incidence of Dental Caries. Trans Edinb Obstet Soc. 1929;49:25-47. PubMed PMID: 29612410
  8. Hense L, Hugger A, Hansson N. Excellence in dental research: nominated scholars for the Nobel Prize 1901-1950 with a focus on Lady May Mellanby (1882-1978) and Walter Hess (1885-1980). Br Dent J. 2022;232(11):825-829. PubMed PMID: 35689067
  9. Hawgood BJ. Sir Edward Mellanby (1884-1955) GBE KCB FRCP FRS: nutrition scientist and medical research mandarin. J Med Biogr. 2010;18(3):150-7. PubMed PMID: 20798415
  10. Rajakumar K. Vitamin D, cod-liver oil, sunlight, and rickets: a historical perspective. Pediatrics. 2003;112(2):e132-5. PubMed PMID: 12897318
  11. Chesney RW. Early animal models of rickets and proof of a nutritional deficiency hypothesis. J Pediatr Gastroenterol Nutr. 2012;54(3):322-7. PubMed PMID: 22134552
  12. Schlemmer U, Frølich W, Prieto RM, Grases F. Phytate in foods and significance for humans: food sources, intake, processing, bioavailability, protective role and analysis. Mol Nutr Food Res. 2009;53 Suppl 2:S330-75. PubMed PMID: 19774556
  13. Gupta RK, Gangoliya SS, Singh NK. Reduction of phytic acid and enhancement of bioavailable micronutrients in food grains. J Food Sci Technol. 2015;52(2):676-84. PubMed PMID: 25694676

PubMed Topic Searches

  1. https://pubmed.ncbi.nlm.nih.gov/?term=Mellanby+E%5BAuthor%5D+rickets
  2. https://pubmed.ncbi.nlm.nih.gov/?term=phytic+acid+calcium+absorption
  3. https://pubmed.ncbi.nlm.nih.gov/?term=Mellanby+M%5BAuthor%5D+teeth
  4. https://pubmed.ncbi.nlm.nih.gov/?term=history+of+rickets+cod+liver+oil

Further Reading

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Connections

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